Research Paper Volume 12, Issue 6 pp 5362—5383

Delphinidin attenuates pathological cardiac hypertrophy via the AMPK/NOX/MAPK signaling pathway

Figure 2. Delphinidin attenuated cardiac hypertrophy and improved cardiac function induced by pressure overload in vivo. (A) Statistical differences in the heart weight/body weight (HW/BW) and heart weight/tibia length (HW/TL) ratios between sham and TAC mice treated with vehicle or delphinidin (n=8). (B) Echocardiographic parameters in sham and TAC mice treated with vehicle or delphinidin (n=8). (C) Left, Hematoxylin-eosin (H&E) staining was performed to assess hypertrophic growth of the hearts of sham and TAC mice treated with vehicle or delphinidin (n=8). Right, Statistical analysis of differences in cardiomyocyte size (n=8). (D) Quantitative dihydroethidium (DHE) staining (n=8). (E) Chemiluminescence lucigenin assay (n=8). (F) Quantitative real-time PCR (qRT-PCR) was performed to analyze the mRNA levels of hypertrophic genes (n=5). In AE, **p<0.01 versus the sham group; ***p<0.001 versus the sham group; ns versus the TAC group; #p<0.05 versus the TAC group; ##p<0.01 versus the TAC group; ###p<0.001 versus the TAC group. qRT-PCR was performed to analyze the mRNA levels of hypertrophic genes (n=5). In AE, **p<0.01 versus the sham group; ***p<0.001 versus the sham group; ns versus the TAC group; #p<0.05 versus the TAC group; ##p<0.01 versus the TAC group; ###p<0.001 versus the TAC group.